Diabetic kidney disease update: Pathogenesis and treatment overview for clinicians (original) (raw)
Related papers
Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment
BioMed Research International, 2021
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. Chronic hyperglycemia and high blood pressure are the main risk factors for the development of DN. In general, screening for microalbuminuria should be performed annually, starting 5 years after diagnosis in type 1 diabetes and at diagnosis and annually thereafter in type 2 diabetes. Standard therapy is blood glucose and blood pressure control using the renin-angiotensin system blockade, targeting A 1 c < 7 % , and <130/80 mmHg. Regression of albuminuria remains an important therapeutic goal. However, there are problems in diagnosis and treatment of nonproteinuric DN (NP-DN), which does not follow the classic pattern of DN. In fact, the prevalence of DN continues to increase, and additional therapy is needed to prevent or ameliorate the condition. In addition to conventional therapies, vitamin D receptor activators, incretin-related drugs, and therapies that target inflammation may also be pro...
Kidney International, 2004
Background. Proteinuria or albuminuria is an established risk marker for progressive renal function loss. Albuminuria can be effectively lowered with antihypertensive drugs that interrupt the renin-angiotensin system (RAS). We investigated whether albuminuria could not only serve as a marker of renal disease, but also function as a monitor of the renoprotective efficacy of RAS intervention by the angiotensin II (Ang II) antagonist, losartan, in patients with diabetic nephropathy.
American Journal of Kidney Diseases, 2005
Background: Little is known of the effects of blood pressure reduction by specific classes of antihypertensive drugs on the association between proteinuria reduction and progression of kidney insufficiency and development of end-stage kidney disease in patients with overt diabetic nephropathy in type 2 diabetes mellitus. Methods: Associations between baseline proteinuria and proteinuria reduction by either irbesartan, amlodipine, or control for similar decrements in blood pressure and the cumulative incidence of renal end points were examined using the Kaplan-Meier method in patients enrolled in the Irbesartan Diabetic Nephropathy Trial. Results: Risk for kidney failure doubled for each doubling of baseline proteinuria level (hazard ratio, 2.04; 95% confidence interval, 1.87 to 2.22; P < 0.001). For each halving of proteinuria level between baseline and 12 months with treatment, risk for kidney failure was reduced by more than half (hazard ratio, 0.44; 95% confidence interval, 0.40 to 0.49; P < 0.001). For the same proportional change in proteinuria, the reduction in risk for kidney failure was significantly greater for irbesartan compared with amlodipine (P ؍ 0.048), but not control (P ؍ 0.245). Proteinuria reduction in the first 12 months of therapy with irbesartan is associated with 36% of the total renoprotective effect observed. Conclusion: Baseline proteinuria is an important risk factor for kidney failure and provides a means to identify patients at greatest risk. Halving proteinuria halves the kidney risk. Proteinuria reduction using an angiotensin receptorblocking agent, such as irbesartan, should be regarded as an important therapeutic goal in renoprotective strategies. Am J Kidney Dis 45:281-287.
Diabetic Proteinuria Revisited: Updated Physiologic Perspectives
Cells
Albuminuria, a hallmark of diabetic nephropathy, reflects not only injury and dysfunction of the filtration apparatus, but is also affected by altered glomerular hemodynamics and hyperfiltration, as well as by the inability of renal tubular cells to fully retrieve filtered albumin. Albuminuria further plays a role in the progression of diabetic nephropathy, and the suppression of glomerular albumin leak is a key factor in its prevention. Although microalbuminuria is a classic manifestation of diabetic nephropathy, often progressing to macroalbuminuria or overt proteinuria over time, it does not always precede renal function loss in diabetes. The various components leading to diabetic albuminuria and their associations are herein reviewed, and the physiologic rationale and efficacy of therapeutic interventions that reduce glomerular hyperfiltration and proteinuria are discussed. With these perspectives, we propose that these measures should be initiated early, before microalbuminuria...
Diabetic nephropathy: Clinical presentation, course, and novel treatment possibilities
Opsta medicina
Diabetic kidney disease (DBD) is one of the major complications of diabetes (DM) and the leading cause of chronic kidney disease (CKD) worldwide. About 10% of patients with DBD progress to terminal HBB, and the rest die mostly due to cardiovascular disorders and infection even before they need treatment for kidney replacement. The main strategies to prevent the development and alleviate the progression of DBB in recent decades have been intensive glycemic control and blockade of the renin-angiotensin-aldosterone system. However, this approach did not achieve optimal results. Taking into account the increase in patients with DBB, high spending from the health care budget and the development of new therapeutic possibilities with significant kidney protection, the International Society of Nephrology issued in 2020. (Kidney Disease: Improving Global Outcomes (KDIGO) Guideline) is the first guide to treating patients with DBB. This review paper aims to point out phenotypic variability an...
Diabetic kidney disease: from physiology to therapeutics
The Journal of Physiology, 2014
Diabetic kidney disease (DKD) defines the functional, structural and clinical abnormalities of the kidneys that are caused by diabetes. This complication has become the single most frequent cause of end-stage renal disease. The pathophysiology of DKD comprises the interaction of both genetic and environmental determinants that trigger a complex network of pathophysiological events, which leads to the damage of the glomerular filtration barrier, a highly specialized structure formed by the fenestrated endothelium, the glomerular basement membrane and the epithelial podocytes, that permits a highly selective ultrafiltration of the blood plasma. DKD evolves gradually over years through five progressive stages. Briefly they are: reversible glomerular hyperfiltration, normal glomerular filtration and normoalbuminuria, normal glomerular filtration and microalbuminuria, macroalbuminuria, and renal failure. Approximately 20-40% of diabetic patients develop microalbuminuria within 10-15 years of the diagnosis of diabetes, and about 80-90% of those with microalbuminuria progress to more advanced stages. Thus, after 15-20 years, macroalbuminuria occurs approximately in 20-40% of patients, and around half of them will present renal insufficiency within 5 years. The screening and early diagnosis of DKD is based on the measurement of urinary albumin excretion and the detection of microalbuminuria, the first clinical sign of DKD. The management of DKD is based on the general recommendations in the treatment of patients with diabetes, including optimal glycaemic and blood pressure control, adequate lipid management and abolishing smoking, in addition to the lowering of albuminuria.
Preventing the progression of diabetic kidney disease
Diabetic kidney disease (DKD) is a progressive condition and is an important cause of end-stage renal disease (ESRD) causing increased morbidity and mortality. The objective of this review article is to discuss about recognition and treatment of early DKD to prevent its progression. Informations have been gathered from related clinical studies, research works, articles, abstracts, and guidelines of different organizations published in various journals. Microalbuminuria describes the urinary excretion of small amounts of albumin which identifies the early stage of DKD. In addition to an earliest marker of kidney damage, microalbuminuria is an established high risk factor for cardiovascular morbidity and mortality. Patients with microalbuminuria who progress to macroalbuminuria are likely to progress to ESRD. There is general agreement that people with diabetes should be screened regularly to detect early markers of kidney damage. Albumin creatinine ratio in a morning urine sample is the preferred method of detecting microalbuminuria in diabetes. There is strong evidence that a number of interventions if initiated at early stage of DKD reduces the risk and slows the progression of kidney damage. People with diabetes and microalbuminuria should be treated with a multifactorial intervention approach to retard the progression of DKD. Studies have clearly demonstrated that the use of angiotensin converting enzyme inhibitors or angiotensin 2 receptor blockers with improved glycemic control, blood pressure control, lipid lowering, aspirin, smoking cessation, exercise programs and dietary intervention reduced the development of overt nephropathy and ESRD.
Proteinuria in Chronic Kidney Disease and its Management
Proteinuria is a marker of kidney damage and an important risk factor for progression of chronic kidney disease as well as cardiovascular morbidity and mortality. Albumin is the principal component of proteinuria in glomerular disease. The presence of persistent albumin in the urine is a clear sign of glomerular abnormality. Microalbuminuria describes the urinary excretion of small amounts of albumin which identifies the very early stage of diabetic kidney disease. The albumin creatinine ratio is the preferred method of detecting microalbuminuria. There is strong evidence that treatment in the early stages of chronic kidney disease reduces progression of kidney damage. The levels of proteinuria in both diabetic and non-diabetic kidney disease at which management should be addressed have been reviewed. This article also reviews the interventions recommended for early stages of chronic kidney disease to reduce the risk of progression to end stage kidney failure. Angiotensin converting enzyme inhibitors and angiotensin 2 receptor blockers are more effective in reducing proteinuria and retarding the progression of kidney disease in comparison to other therapies which lower systemic blood pressure to a similar degree.